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Adenylate
cyclase type 2
GABAA receptor
Gamma-
aminobutyric
acid type B
receptor
N-type calcium
channel
G protein-
activated
inward
rectifier
potassium
channel 1
Substance-P
receptor
Mu-type opioid
receptor
Gβ
Gγ
γ-Aminobutyric acid
Substance P
3-Methylthiofentanyl
cAMP
Ca
+
Ca
+
Na
+
Na
+
γ-Aminobutyric acid
3-Methylthiofentanyl
3-Methylthiofentanyl
ATP
PP
i
GTP
Pain
Guanine
nucleotide-
binding protein
G(i) subunit
alpha-1
Magnesium
Less GABA leads to
disinhibition of dopamine
cell firing in the spinal
chord pain transmission
neurons. This leads to less
pain signalling and
analgesia
Decreased calcium levels
lead to decreased
neurotransmitter release.
Less GABA is released for
synaptic vesicles.
3-Methylthiofentanyl
activates presynaptic mu
opioid type receptors in the
dorsal root ganglion
The Gi subunit of the mu
opioid receptor activates
the inwardly rectifying
potassium channel increasing
K+ conductance. This causes
membrane hyperpolarization
decreasing the chances of
neuronal firing/action
potential.
Post-Synaptic Neuron
Pre-Synaptic Neuron
Synapse
Cytosol
Synaptic Vesicle
The mu opioid receptor
through the gamma subunit
inhibits voltage gated
N-type calcium channels
stopping the influx of
calcium into the neuron.
Methadone acts at A delta
and C pain fibres in the
dorsal horn of the spinal
chord. By decreasing
neurotransmitter action
there is less pain
transmittance into the
spinal chord. This leads to
less pain perception.
C Pain Fibres
The inhibition of adenylate
cyclase prevents the
production of cAMP which
further prevents
depolarization and pain
signalling
Substance P is also not
released into the synapse
which prevents the
activation of pain
signalling.
ADCY2
GABRG2
GABBR1
CACNA1B
KCNJ3
TACR1
OPRM1
GNB1
GNG2
γ-Aminobutyric
acid
Substance P
3-
Methylthiofentanyl
cAMP
Calcium
Calcium
Sodium
Sodium
γ-Aminobutyric
acid
3-
Methylthiofentanyl
3-
Methylthiofentanyl
Adenosine
triphosphate
Pyrophosphate
Guanosine
triphosphate
Pain
GNAI1
ADCY2
GABRG2
GABBR1
CACNA1B
KCNJ3
TACR1
OPRM1
GNB1
GNG2
GABA
SP